JoVE Clinical and Translational Medicine
Nadine Nelson, Karoly Szekeres, Denise Cooper, Tomar Ghansah
Department of Molecular Medicine, University of South Florida Morsani College of Medicine
Detta är en snabb och omfattande metod för immunofenotypning Myeloida Härledda suppressorceller (MDSC) och berikande Gr-1
Immunity. Sep, 2003 | Pubmed ID: 14499117
Antigen-presenting cells (APCs) can induce T cell activation as well as T cell tolerance. The molecular mechanisms by which APCs regulate this critical decision of the immune system are not well understood. Here we show that Stat3 signaling plays a critical role in the induction of antigen-specific T cell tolerance. Targeted disruption of Stat3 signaling in APCs resulted in priming of antigen-specific CD4(+) T cells in response to an otherwise tolerogenic stimulus in vivo. Furthermore, APCs devoid of Stat3 effectively break antigen-specific T cell anergy in vitro. Conversely, increased Stat3 activity in APCs led to impaired antigen-specific T cell responses. Stat3 signaling provides, therefore, a novel molecular target for manipulation of immune activation/tolerance, a central decision with profound implications in autoimmunity, transplantation, and cancer immunotherapy.